Chronic kidney disease and ESRD Flashcards Preview

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Flashcards in Chronic kidney disease and ESRD Deck (11)
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1
Q

CKD

A

-A decrement in GFR <15

2
Q

Risk factors of CKD

A
  • Most important cause of CKD is diabetes
  • Proteinuria
  • HTN: goal for BP isnt as large of a risk factor w/o proteinuria
  • But w/ proteinuria HTN is a substantial negative risk factor
3
Q

Rx of CKD and prevention

A
  • Rx the underlying cause of the disease

- This includes giving ACEIs/ARBs, statins for hyperlipidemia

4
Q

Complications of CKD

A
  • Metabolic derangements
  • CV complications
  • CKD mineral bone d/o
  • Anemia, platelet dyfxn
  • Metabolic complications arise as GFR declines and excretion of certain solutes declines as well
  • Impaired excretion of: Na, K, PO4, H+, uric acid
  • Also impaired urinary dilution and concentration
5
Q

Clinical manifestations and lab findings

A
  • Manifestations: fatigue, weakness, pruritus, pallor, anorexia, nausea, vomiting, insomnia, irritability, confusion, hyperreflexia, dyspnea, edema, pericarditis
  • Labs: metabolic acidosis, hyperphosphatemia, hypocalcemia, hyperkalemia, anemia, hyperuricemia, broad waxy casts
6
Q

CVD complications from CKD

A
  • IHD: accelerated atherosclerosis
  • HF: chronic volume overload, vascular calcification, cardiac ischemia
  • Arrhythmias: cardiac remodeling + metabolic derangements
7
Q

CKD mineral bone d/o (secondary hyperparathyroidism)

A
  • PTH levels rise in CKD due to the combination of: decreased vit D, hyperphosphatemia, hypocalcemia
  • Hypocalcemia (due to low levels of vit D- made in PT) leads to increase in PTH release (PTH increases bone turnover to release Ca and PO4 into blood)
  • W/ declining GFR excretion of PO4 decreases
  • High PO4 levels further stimulate PTH and increases FGF23 levels to increase renal PO4 excretion
  • The kidney, however, cannot excrete the PO4 appropriately so PO4 levels remain high
  • FGF23 also normally inhibits PTH release, however in the setting of CKD there is both high FGF23 and PTH thus the parathyroids become resistant to the FGF23
8
Q

Bone d/o in CKD

A
  • Osteitis fibrosa cystica: high bone turnover w/ increased PTH
  • Increased osteoclast activity causes an irregular woven collagen matrix thats weak
  • Adynamic bone: low bone turnover, w/ low PTH
  • Overall little bone formation
9
Q

Management of secondary hyperparathyroidism

A
  • Restrict PO4 in diet
  • PO4 binders w/ meals
  • Screen for vit D deficiency and Rx
  • Monitor PTH, correct hypocalcemia
10
Q

Anemia of CKD

A
  • EPO deficiency: normocytic anemia
  • Anemia more prevalent when GFR <30
  • CKD pts have impaired Fe absorption (mediated by hepcidin)
  • Can give EPO, but has adverse effects: HTN, stroke, thrombosis, RBC aplasia, Fe deficiency, malignancies
11
Q

Rx options for ESRD

A
  • Hemodialysis or peritoneal dialysis
  • Principles of Rx: solute clearance and volume removal
  • Primary mechanism of solute removal is diffusion
  • Primary mechanism of fluid removal is hydrostatic pressure
  • Diffusion is used to achieve desired electrolyte concentrations (i.e. can give back Ca by using a high Ca dialysate)
  • Peritoneal dialysis: blood is filtered indirectly (peritoneal membrane is filter
  • Diffusion occurs btwn blood in the capillaries of the peritoneal membrane and dialysate in the peritoneum